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Delayed postanoxic encephalopathy secondary to acute cocaine and heroin intoxication
European Journal of Radiology Extra 71 (2009) e43–e45
Contents lists available at ScienceDirect
European Journal of Radiology Extra journal homepage: intl.elsevierhealth.com/journals/ejrex
Delayed postanoxic encephalopathy secondary to acute cocaine and heroin intoxication Mireia Moragas a,∗ , Jordi Gascón-Bayarri a , Mònica Cos b , Montserrat Juncadella a , ˜ a , Francisco Rubio a Ramón René a b
Department of Neurology, IDIBELL, Bellvitge University Hospital, L’Hospitalet del Llobregat, Spain Department of Neuroradiology, “Institut de Diagnòstic per la Imatge” in Bellvitge University Hospital, Spain
a r t i c l e
i n f o
Article history: Received 17 July 2008 Received in revised form 6 February 2009 Accepted 5 March 2009 Keyword: Delayed postanoxic encephalopathy
a b s t r a c t Delayed postanoxic encephalopathy (DPE) is a rare condition that presents after apparent recovery from acute cerebral anoxia. DPE, which consists of cognitive and neuropsychiatric deficits, appears between one and three weeks after cerebral anoxia. We present a patient with DPE secondary to acute cocaine and heroin intoxication with typical cranial MRI changes. The clinical improvement of the patient could be related to the improvement in white matter lesions despite the characteristics of the ADC map. © 2009 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Delayed postanoxic encephalopathy (DPE) is a rare condition that presents after apparent recovery from acute cerebral anoxia [1,2,3]. DPE, which consists of cognitive and neuropsychiatric deficits, appears between one and three weeks after cerebral anoxia [1,2]. This condition has been commonly related to carbon monoxide (CO) poisoning [3]. We present a patient with DPE secondary to acute cocaine and heroin intoxication. 2. Materials and methods A 34-year-old man with a history of weekly inhaled cocaine use was found unconscious at home. At the emergency department he showed progressive improvement and became asymptomatic. The neurological examination was normal. Urine tested positive for heroin and cocaine. The absence of other risk factors causing respiratory depression and the prolonged improvement during his observation at the emergency department enabled us to establish a diagnosis of acute respiratory depression secondary to drug abuse. Two weeks later he presented progressive deterioration in his performance at work, memory loss, attentional deficits, indifference, irritability and dysarthria. The neurological examination revealed bilateral asterixis, anterograde memory disorder, attentional deficit and anosognosia and the Mini-Mental test was 17/30. Cranial CT showed bipallidal hypodensity. Cranial MRI (Fig. 1) revealed diffuse
∗ Corresponding author. Tel.: +34 932607711; fax: +34 932607365. E-mail address: [email protected] (M. Moragas). 1571-4675/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejrex.2009.03.004
supratentorial leukoencephalopathy, mainly in the frontoparietal region, consisting of high signal intensity areas in T2-weighted, FLAIR and isotropic diffusion-weighted images (DWI) with low ADC values. There was high signal intensity in FLAIR and T2-weighted images in both pallidal nuclei. Neuropsychological examination showed a frontal dysexecutive syndrome with moderate memory deficits. One month later, both the patient and his family reported a subjective improvement (greater ability to concentrate and retain new information). The cranial MRI (Fig. 2) showed a reduction in the damage to white matter of the bilateral frontal corona radiata and pallidal nuclei, with persistent high signal intensity in DWI images. The ADC value continued to be low. Neuropsychological examination revealed an improvement in the dysexecutive syndrome at the expense of language fluency, capacity for abstract thought and immediate and delayed memory.
3. Discussion DPE has an insidious onset characterized by personality and behavioural changes and movement disorders. It begins with apathy, confusion, attentional and memory deficits, irritability and aggressiveness followed by altered gait, spasticity, sphincter incontinence and extrapyramidal and speech disorders, leading eventually to coma or death of the patient [2,3]. These disorders may stabilize, leaving behind a certain degree of deterioration, or could result in a significant improvement [1]. It has been related to acute CO poisoning [3] (2.75% of cases of CO poisoning [6]), to connatal and post-surgical anoxia, cardiorespiratory arrest of any
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M. Moragas et al. / European Journal of Radiology Extra 71 (2009) e43–e45
Fig. 1. Initial magnetic resonance imaging findings. FLAIR images (a) show high signal intensity areas in the bilateral periventricular white matter and pallidal nuclei. DWI imaging (b) show similar high signal intensity in the periventricular white matter, with diffuse low signal intensity in the ADC map (c).
cause (cardiac disease, heroin intoxication [6]), hypovolemic shock, hypoglycemia and strangulation [1,4,5]. Of all the neurologic complications due to heroin use, DPE has been the least common [6], although hypoxia induced by heroin is not so rare. Other more frequent neurological complications after heroin abuse are acute paraplegia caused by transverse myelitis or epidural abscess, painful mononeuropathy and cerebral edema
after hypersensibility reactions to impurities used to dilute heroin [6]. Two types of histopathological patterns have been reported in the literature. One pattern comprises different degrees of demyelinization in the centrum semiovale and the other one entails degeneration of the cortical laminae and basal ganglia. This two patterns correlate with cranial MRI [1,5]. Some authors consider
Fig. 2. Follow-up magnetic resonance, one month later, shows a reduction of white matter damage of the bilateral frontal corona radiata and pallidal nuclei (a), and persistence of DWI findings (b) with diffuse low signal intensity in the ADC map (c).
M. Moragas et al. / European Journal of Radiology Extra 71 (2009) e43–e45
that the presence of necrotic lesions is related to acute postanoxic encephalopathy and that demyelinating lesions are a sign of DPE [7,8]. The physiopathogenic mechanism of these lesions remains unclear although two main hypotheses have been proposed: neuronal apoptosis [9,10] and demyelinization [11]. In DPE, the initial anoxia should be severe enough for a threshold to be exceeded triggering apoptosis, which leads to neuronal death. The demyelinization visible in cranial MRI is attributed to oligodendroglial dysfunction and attempts have been made to relate this to an arylsulphatase A deficiency [11]. A number of studies describe DPE neuroimaging, which consists of (1) an increased signal in T2-weighted and FLAIR images with repercussions in the diffusion-weighted images and ADC map in centrum semiovale and periventricular white matter, and (2) an altered bipallidal signal with low signal intensity in T1-weighted and high signal intensity in T2-weighted and FLAIR images [12,13]. It is reasonable to assume that images in pallidal nuclei are secondary to acute damage after anoxic injury, whereas images in white matter correspond to delayed damage. Radiologic imaging of the patient and his evolution are different from those described in chronic drug users such as microvascular ischemic changes, or ischemic stroke. A rare form of leukoencephalopathy has been reported in abusers who inhale heroin vapors. Atrophy has also been described [14]. The results of the DWI images and the ADC map of the present case correlate with the findings observed in other series of delayed encephalopathy of acute carbon monoxide intoxication [12]. The restricted diffusion of the white matter lesion develops late after the patient’s exposure to cocaine and heroin and persists longer than the usual two to three weeks after an acute ischemic infarct. The prognosis varies between death and complete recovery. A good evolution (50–75%) is not related to medication [1,8]. Severity and persistence of DPE sequelae have been related to the presence and persistence of low signal intensity in the ADC map of the cranial MRI [12]. The patient’s outcome was favourable and coincided with an improvement in the white matter lesions in the FLAIR images despite the presence and persistence of low signal intensity in the ADC map.
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In conclusion, delayed postanoxic encephalopathy should be suspected in patients who have suffered respiratory depression, and the appropriate measures should be taken. The clinical evolution of this condition may be favourable and could be related to an improvement in white matter lesions despite the characteristics of the ADC map. Conflict of interest None. References [1] Custodio CM, Basford JR. Delayed postanoxic encephalopathy: a case report and literature review. Arch Phys Med Rehabil 2004;85:502–5. [2] Plum F, Posner JB, Hain RF. Delayed neurological deterioration after anoxia. Arch Inter Med 1962;110:18–25. [3] Choi IS. Delayed neurologic sequelae in carbon monoxide intoxication. Arch Neurol 1983;40:433–5. [4] Ginsberg MD. Delayed neurological deterioration following hypoxia. Adv Neurol 1979;26:21–44. [5] Hori A, Hirose G, Kataoka S, et al. Delayed postanoxic encephalopathy after strangulation: serial neuroradiological and neurochemical studies. Arch Neurol 1991;48:871–4. [6] Protass LM. Delayed Postanoxic Encephalopathy after heroin use. Ann Int Med 1971;74:738–9. [7] Choi IS, Kim SK, Choi YC, et al. Evaluation of outcome after acute carbon monoxide poisoning by brain CT. J Korean Med Sci 1993;8:78–83. [8] Kwon OY, Chung SP, Ha R, et al. Delayed postanoxic encephalopathy after carbon monoxide poisoning. Emerg Med J 2004;21:250–1. [9] Sheth RD, Bodensteiner JB. Delayed postanoxic encephalopathy: possible role for apoptosis. J Child Neurol 1998;13:347–8. [10] Kim HY, Kim BJ, Moon SY, et al. Serial diffusion-weighted MR imaging in delayed postanoxic encephalopathy. A case study. J Neuroradiol 2002;29(3): 211–5. [11] Barker RA, Dick DJ, Cochius JI. Delayed postanoxic encephalopathy and pseudodeficiency of arylsulphatase A. J Neurol 1999;246:1103–4. [12] Kim JH, Chang KH, Song IC, et al. Delayed encephalopathy of acute carbon monoxide intoxication: diffusivity of cerebral white matter lesions. Am J Neuroradiol 2003;24:1592–7. [13] Inagaki T, Ishino H, Seno H, et al. A long-term study of serial magnetic resonance images en patients with delayed encephalopathy after acute carbon monoxide poisoning. Psychiatry Clin Neurosci 1997;51(6):421–3. [14] Borne J, Riascos R, Cuellar H, et al. Neuroimaging in drug and substance abuse part II: opioids and solvents. Top Magn Reson Imaging 2005;16(3):239–45.
Contents lists available at ScienceDirect
European Journal of Radiology Extra journal homepage: intl.elsevierhealth.com/journals/ejrex
Delayed postanoxic encephalopathy secondary to acute cocaine and heroin intoxication Mireia Moragas a,∗ , Jordi Gascón-Bayarri a , Mònica Cos b , Montserrat Juncadella a , ˜ a , Francisco Rubio a Ramón René a b
Department of Neurology, IDIBELL, Bellvitge University Hospital, L’Hospitalet del Llobregat, Spain Department of Neuroradiology, “Institut de Diagnòstic per la Imatge” in Bellvitge University Hospital, Spain
a r t i c l e
i n f o
Article history: Received 17 July 2008 Received in revised form 6 February 2009 Accepted 5 March 2009 Keyword: Delayed postanoxic encephalopathy
a b s t r a c t Delayed postanoxic encephalopathy (DPE) is a rare condition that presents after apparent recovery from acute cerebral anoxia. DPE, which consists of cognitive and neuropsychiatric deficits, appears between one and three weeks after cerebral anoxia. We present a patient with DPE secondary to acute cocaine and heroin intoxication with typical cranial MRI changes. The clinical improvement of the patient could be related to the improvement in white matter lesions despite the characteristics of the ADC map. © 2009 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Delayed postanoxic encephalopathy (DPE) is a rare condition that presents after apparent recovery from acute cerebral anoxia [1,2,3]. DPE, which consists of cognitive and neuropsychiatric deficits, appears between one and three weeks after cerebral anoxia [1,2]. This condition has been commonly related to carbon monoxide (CO) poisoning [3]. We present a patient with DPE secondary to acute cocaine and heroin intoxication. 2. Materials and methods A 34-year-old man with a history of weekly inhaled cocaine use was found unconscious at home. At the emergency department he showed progressive improvement and became asymptomatic. The neurological examination was normal. Urine tested positive for heroin and cocaine. The absence of other risk factors causing respiratory depression and the prolonged improvement during his observation at the emergency department enabled us to establish a diagnosis of acute respiratory depression secondary to drug abuse. Two weeks later he presented progressive deterioration in his performance at work, memory loss, attentional deficits, indifference, irritability and dysarthria. The neurological examination revealed bilateral asterixis, anterograde memory disorder, attentional deficit and anosognosia and the Mini-Mental test was 17/30. Cranial CT showed bipallidal hypodensity. Cranial MRI (Fig. 1) revealed diffuse
∗ Corresponding author. Tel.: +34 932607711; fax: +34 932607365. E-mail address: [email protected] (M. Moragas). 1571-4675/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejrex.2009.03.004
supratentorial leukoencephalopathy, mainly in the frontoparietal region, consisting of high signal intensity areas in T2-weighted, FLAIR and isotropic diffusion-weighted images (DWI) with low ADC values. There was high signal intensity in FLAIR and T2-weighted images in both pallidal nuclei. Neuropsychological examination showed a frontal dysexecutive syndrome with moderate memory deficits. One month later, both the patient and his family reported a subjective improvement (greater ability to concentrate and retain new information). The cranial MRI (Fig. 2) showed a reduction in the damage to white matter of the bilateral frontal corona radiata and pallidal nuclei, with persistent high signal intensity in DWI images. The ADC value continued to be low. Neuropsychological examination revealed an improvement in the dysexecutive syndrome at the expense of language fluency, capacity for abstract thought and immediate and delayed memory.
3. Discussion DPE has an insidious onset characterized by personality and behavioural changes and movement disorders. It begins with apathy, confusion, attentional and memory deficits, irritability and aggressiveness followed by altered gait, spasticity, sphincter incontinence and extrapyramidal and speech disorders, leading eventually to coma or death of the patient [2,3]. These disorders may stabilize, leaving behind a certain degree of deterioration, or could result in a significant improvement [1]. It has been related to acute CO poisoning [3] (2.75% of cases of CO poisoning [6]), to connatal and post-surgical anoxia, cardiorespiratory arrest of any
e44
M. Moragas et al. / European Journal of Radiology Extra 71 (2009) e43–e45
Fig. 1. Initial magnetic resonance imaging findings. FLAIR images (a) show high signal intensity areas in the bilateral periventricular white matter and pallidal nuclei. DWI imaging (b) show similar high signal intensity in the periventricular white matter, with diffuse low signal intensity in the ADC map (c).
cause (cardiac disease, heroin intoxication [6]), hypovolemic shock, hypoglycemia and strangulation [1,4,5]. Of all the neurologic complications due to heroin use, DPE has been the least common [6], although hypoxia induced by heroin is not so rare. Other more frequent neurological complications after heroin abuse are acute paraplegia caused by transverse myelitis or epidural abscess, painful mononeuropathy and cerebral edema
after hypersensibility reactions to impurities used to dilute heroin [6]. Two types of histopathological patterns have been reported in the literature. One pattern comprises different degrees of demyelinization in the centrum semiovale and the other one entails degeneration of the cortical laminae and basal ganglia. This two patterns correlate with cranial MRI [1,5]. Some authors consider
Fig. 2. Follow-up magnetic resonance, one month later, shows a reduction of white matter damage of the bilateral frontal corona radiata and pallidal nuclei (a), and persistence of DWI findings (b) with diffuse low signal intensity in the ADC map (c).
M. Moragas et al. / European Journal of Radiology Extra 71 (2009) e43–e45
that the presence of necrotic lesions is related to acute postanoxic encephalopathy and that demyelinating lesions are a sign of DPE [7,8]. The physiopathogenic mechanism of these lesions remains unclear although two main hypotheses have been proposed: neuronal apoptosis [9,10] and demyelinization [11]. In DPE, the initial anoxia should be severe enough for a threshold to be exceeded triggering apoptosis, which leads to neuronal death. The demyelinization visible in cranial MRI is attributed to oligodendroglial dysfunction and attempts have been made to relate this to an arylsulphatase A deficiency [11]. A number of studies describe DPE neuroimaging, which consists of (1) an increased signal in T2-weighted and FLAIR images with repercussions in the diffusion-weighted images and ADC map in centrum semiovale and periventricular white matter, and (2) an altered bipallidal signal with low signal intensity in T1-weighted and high signal intensity in T2-weighted and FLAIR images [12,13]. It is reasonable to assume that images in pallidal nuclei are secondary to acute damage after anoxic injury, whereas images in white matter correspond to delayed damage. Radiologic imaging of the patient and his evolution are different from those described in chronic drug users such as microvascular ischemic changes, or ischemic stroke. A rare form of leukoencephalopathy has been reported in abusers who inhale heroin vapors. Atrophy has also been described [14]. The results of the DWI images and the ADC map of the present case correlate with the findings observed in other series of delayed encephalopathy of acute carbon monoxide intoxication [12]. The restricted diffusion of the white matter lesion develops late after the patient’s exposure to cocaine and heroin and persists longer than the usual two to three weeks after an acute ischemic infarct. The prognosis varies between death and complete recovery. A good evolution (50–75%) is not related to medication [1,8]. Severity and persistence of DPE sequelae have been related to the presence and persistence of low signal intensity in the ADC map of the cranial MRI [12]. The patient’s outcome was favourable and coincided with an improvement in the white matter lesions in the FLAIR images despite the presence and persistence of low signal intensity in the ADC map.
e45
In conclusion, delayed postanoxic encephalopathy should be suspected in patients who have suffered respiratory depression, and the appropriate measures should be taken. The clinical evolution of this condition may be favourable and could be related to an improvement in white matter lesions despite the characteristics of the ADC map. Conflict of interest None. References [1] Custodio CM, Basford JR. Delayed postanoxic encephalopathy: a case report and literature review. Arch Phys Med Rehabil 2004;85:502–5. [2] Plum F, Posner JB, Hain RF. Delayed neurological deterioration after anoxia. Arch Inter Med 1962;110:18–25. [3] Choi IS. Delayed neurologic sequelae in carbon monoxide intoxication. Arch Neurol 1983;40:433–5. [4] Ginsberg MD. Delayed neurological deterioration following hypoxia. Adv Neurol 1979;26:21–44. [5] Hori A, Hirose G, Kataoka S, et al. Delayed postanoxic encephalopathy after strangulation: serial neuroradiological and neurochemical studies. Arch Neurol 1991;48:871–4. [6] Protass LM. Delayed Postanoxic Encephalopathy after heroin use. Ann Int Med 1971;74:738–9. [7] Choi IS, Kim SK, Choi YC, et al. Evaluation of outcome after acute carbon monoxide poisoning by brain CT. J Korean Med Sci 1993;8:78–83. [8] Kwon OY, Chung SP, Ha R, et al. Delayed postanoxic encephalopathy after carbon monoxide poisoning. Emerg Med J 2004;21:250–1. [9] Sheth RD, Bodensteiner JB. Delayed postanoxic encephalopathy: possible role for apoptosis. J Child Neurol 1998;13:347–8. [10] Kim HY, Kim BJ, Moon SY, et al. Serial diffusion-weighted MR imaging in delayed postanoxic encephalopathy. A case study. J Neuroradiol 2002;29(3): 211–5. [11] Barker RA, Dick DJ, Cochius JI. Delayed postanoxic encephalopathy and pseudodeficiency of arylsulphatase A. J Neurol 1999;246:1103–4. [12] Kim JH, Chang KH, Song IC, et al. Delayed encephalopathy of acute carbon monoxide intoxication: diffusivity of cerebral white matter lesions. Am J Neuroradiol 2003;24:1592–7. [13] Inagaki T, Ishino H, Seno H, et al. A long-term study of serial magnetic resonance images en patients with delayed encephalopathy after acute carbon monoxide poisoning. Psychiatry Clin Neurosci 1997;51(6):421–3. [14] Borne J, Riascos R, Cuellar H, et al. Neuroimaging in drug and substance abuse part II: opioids and solvents. Top Magn Reson Imaging 2005;16(3):239–45.